Sigma-1 receptor antagonismpromotes long-trace ethanolinduced conditioned tasteaversion in adolescent rats

  1. Salguero, Agustín 1
  2. Mujica, Victoria 1
  3. Ruiz-Leyva, Leandro 2
  4. Morón Henche, Ignacio 3
  5. Cendán, Cruz Miguel 2
  6. Marengo, Leonardo 1
  7. Moreno, Paloma 1
  8. Pautassi, Ricardo 1
  1. 1 Instituto de Investigación Médica M. y M. Ferreyra (INIMEC –CONICET-Universidad Nacional de Córdoba)
  2. 2 Department of Pharmacology, Institute of Neuroscience, Biomedical Research Center (CIBM) Faculty of Medicine, University of Granada, Spain
  3. 3 Department of Psychobiology and Centre of Investigation of Mind, Brain, and Behavior (CIMCYC), Faculty of Psychology, University of Granada, Spain
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Journal:
Revista Argentina de Ciencias del Comportamiento ( RACC )

ISSN: 1852-4206

Year of publication: 2024

Issue Title: Actas de resúmenes de la XIX Reunión Nacional y VIII Encuentro Internacional de la Asociación Argentina de Ciencias del Comportamiento

Volume: 16

Issue: 3

Pages: 149-150

Type: Article

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Abstract

Introduction:Previous studies suggest that the Sigma receptor system is involved in the motivational effects of ethanol. Objective:we examined, in adolescent rats, the involvement of the sigma 1 receptor (S1-R) antagonist S1RA in an ethanol-induced conditioned taste aversion (CTA). Methods: we studied the role of S1RA in an ethanol-induced CTA in which the Conditioned Stimulus (CS, saccharine, 0.1%) was presented immediately before the Unconditioned Stimulus (US, ethanol, 2.5 g/kg) or with a CS-US interval of 30 minutes. Results:In Experiment 1we found that administration of S1RA (4 or 16 mg/kg, administered 30 min before alcohol) did not alter the expression or extinction of ethanol-induced CTA. A second phase of this experiment tested control rats (i.e., those administered with 0 g/kg alcoholat the previous phase) for lithium-chloride–induced CTA (like in the previous phase, the CS was presented immediately before the US), which was not affected by S1RA (16 mg/kg). In Experiment 2 we inserted a 30 min interval between CS and US, and this resulted in the absence of ethanol-induced CTA. Administration of S1RA (16 mg/kg) before alcohol, however, promoted the expression of this long-trace ethanol-induced CTA at adolescence. Intriguingly, we found that rats given S1RA at conditioning (PD30) did notexhibit ethanol-induced locomotor activity, when assessed later at adolescence (PD39). Administration of S1RA (16 mg/kg) did not affect mean alcohol blood levels at PD30. Discussion:These results suggest that S1-R antagonism, at adolescence, might block the appetitive effects of ethanol and, therefore, exacerbate the aversive effects of this drug.

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